# Synucleinopathy

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Medical condition

Synucleinopathy Other names α-synucleinopathies Positive α-synuclein staining (brown) of a Lewy body in the substantia nigra of an individual with Parkinson's disease Specialty Neurology Symptoms Autonomic dysfunction, motor impairments, cognitive and sleep issues, parkinsonism, memory loss, hallucinations Duration Long term Types Parkinson's disease, dementia with Lewy bodies, multiple system atrophy Causes Unknown

**Synucleinopathies** are [neurodegenerative](/source/Neurodegenerative) diseases characterised by the abnormal accumulation of aggregates of [alpha-synuclein protein](/source/Alpha-synuclein) in neurons, nerve fibres or [glial](/source/Glia) cells.[1] The synucleinopathies include [Parkinson's disease](/source/Parkinson's_disease) (PD), [dementia with Lewy bodies](/source/Dementia_with_Lewy_bodies) (DLB), and [multiple system atrophy](/source/Multiple_system_atrophy) (MSA).[1] Other rare disorders, such as various neuroaxonal dystrophies, also have α-synuclein pathologies.[2]

## Classification

The synucleinopathies include [Parkinson's disease](/source/Parkinson's_disease) (PD), [dementia with Lewy bodies](/source/Dementia_with_Lewy_bodies) (DLB), and [multiple system atrophy](/source/Multiple_system_atrophy) (MSA).[1] Other rare disorders, such as various neuroaxonal dystrophies, also have α-synuclein pathologies.[2]

## Signs and symptoms

The synucleinopathies have shared features of [parkinsonism](/source/Parkinsonism), impaired cognition, [sleep disorders](/source/Sleep_disorder), and [visual hallucinations](/source/Visual_hallucination).[3]

Synucleinopathies can overlap with [tauopathies](/source/Tauopathies), possibly because of interaction between the synuclein and [tau](/source/Tau_protein) proteins.[4]

[REM sleep behavior disorder](/source/REM_sleep_behavior_disorder) (RBD) is a [parasomnia](/source/Parasomnia) in which individuals with RBD lose the paralysis of muscles (atonia) that is normal during [rapid eye movement (REM) sleep](/source/Rapid_eye_movement_sleep), and act out their dreams or have other abnormal movements or vocalizations.[5] Abnormal sleep behaviors may appear decades before any other symptoms, often as an [early sign](/source/Prodome) of a synucleinopathy.[6] On autopsy, 94 to 98% of individuals with [polysomnography](/source/Polysomnography)-confirmed RBD are found to have a synucleinopathy—most commonly DLB or PD.[5][7][8] Other symptoms of the specific synucleinopathy usually manifest within 15 years of the diagnosis of RBD,[9] but may emerge up to 50 years after RBD diagnosis.[5]

Alpha-synuclein deposits can affect the [cardiac muscle](/source/Myocard) and blood vessels.[10] Almost all people with synucleinopathies have cardiovascular dysfunction, although most are asymptomatic.[10]

From chewing to [defecation](/source/Defecation), alpha-synuclein deposits affect every level of gastrointestinal function. Symptoms include upper [gastrointestinal tract](/source/Gastrointestinal_tract) dysfunction such as [delayed gastric emptying](/source/Gastroparesis) or lower gastrointestinal dysfunction, such as constipation and prolonged stool transit time.[10]

[Urinary retention](/source/Urinary_retention), [waking at night to urinate](/source/Nocturia), increased urinary frequency and urgency, and over- or underactive bladder are common in people with synucleinopathies.[10] Sexual dysfunction usually appears early in synucleinopathies, and may include [erectile dysfunction](/source/Erectile_dysfunction), and difficulties achieving [orgasm](/source/Orgasm) or [ejaculating](/source/Ejaculation).[10]

## Mechanism

The [pathological](/source/Pathology) aggregation of alpha-synuclein plays a key role in neurodegenerative disease.[11] The misfolding and aggregation of alpha-synuclein form [toxic fibrils](/source/Fibril), which in turn form pathological inclusions, such as [Lewy bodies](/source/Lewy_body).[12] These protein deposits are a hallmark of synucleinopathies, and may interrupt crucial neuronal processes, such as functions of [synaptic vesicles](/source/Synaptic_vesicle), leading to neuronal death.[11] While PD and DLB are characterized by neuronal aggregates of alpha-synuclein, MSA is characterized by glial aggregates, featuring glial cytoplasmic inclusions rather than Lewy bodies.[13]

Alpha-synuclein is encoded by the *SNCA* [gene](/source/Gene), and rare mutations in this gene can lead to dysfunctions of the [protein structure](/source/Protein_structure).[14] [Post-translational modifications](/source/Post-translational_modification) are also implicated in the aggregation of alpha-synuclein, mostly occurring in the [C-terminus](/source/C-terminus). Phosphorylation, acetylation, ubiquitination, oxidation, and other modifications alter the structure and charge of alpha-synuclein, which can in turn lead to the formation of Lewy bodies.[15]

Alpha-synuclein has a [prion-like](/source/Prion) molecular spread and is suggested to be released through rare [exocytosis](/source/Exocytosis) pathways.[15] This release with [exosomes](/source/Exosome_(vesicle)) on their way to degradation in [lysosomes](/source/Lysosome) suggests this process may be calcium-dependent, and therefore suggests propagation of misfolded alpha-synuclein between neurons synaptically connected.[15] Neuronal death caused by aggregated alpha-synuclein may also further accelerate the formation of these toxic aggregates, which can then trigger a selective progression of neuronal death through impairment of the [mitochondria](/source/Mitochondrion), alteration of [calcium homeostasis](/source/Calcium_metabolism), and lysosomal dysfunction.[14][16]

Early synaptic and [plastic](/source/Neuroplasticity) alterations mediated by alpha-synuclein, as well as the mechanisms of inflammation and synaptic dysfunction that occurs before [neurodegeneration](/source/Neurodegeneration), are of key interest for investigating possible therapies for synucleinpathies.[16]

## Diagnosis

### Differential diagnosis

Persons with PD are typically less caught up in their visual hallucinations than those with DLB.[17] There is a lower incidence of tremor at rest in DLB than in PD, and signs of parkinsonism in DLB are more symmetrical.[6] In MSA, [autonomic dysfunction](/source/Dysautonomia) appears earlier and is more severe, and is accompanied by uncoordinated movements, while visual hallucinations and fluctuating cognition are less common than in DLB.[18] Urinary difficulties are one of the earliest symptoms with MSA, and are often severe.[10]

## Management

As of 2016, there are no medications that stop or improve the progression of synucleinopathies; treatments are limited to managing symptoms.[19] Symptomatic therapies include medications for motor symptoms, treatments for autonomic dysfunction, and management of sleep or cognitive problems.[10] [Non-pharmacological](/source/Non-pharmacological_intervention) approaches such as [physical therapy](/source/Physical_therapy), [occupational therapy](/source/Occupational_therapy), and [speech therapy](/source/Speech%E2%80%93language_pathology) are also commonly used.[10][20]

Since alpha-synuclein is involved in the synucleinopathies, many potential [disease-modifying treatments](/source/Disease-modifying_treatment) target this protein and its role in early inflammation and synaptic dysfunction.[19]

## See also

- [Proteopathy](/source/Proteopathy)

- [Anti-α-synuclein drug](/source/Anti-%CE%B1-synuclein_drug)

## References

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v t e Diseases of the nervous system, primarily CNS Inflammation Brain Encephalitis Viral encephalitis Herpesviral encephalitis Limbic encephalitis Encephalitis lethargica Cavernous sinus thrombosis Brain abscess Amoebic Brain and spinal cord Encephalomyelitis Acute disseminated Meningitis Meningoencephalitis Brain/ encephalopathy Degenerative Extrapyramidal and movement disorders Basal ganglia disease Parkinsonism PD Postencephalitic NMS PSP CBD NBIA PKAN Striatonigral degeneration Hemiballismus Huntington's disease Olivopontocerebellar atrophy Dyskinesia Dystonia Status dystonicus Spasmodic torticollis Meige's Blepharospasm Athetosis Chorea Choreoathetosis Myoclonus Myoclonic epilepsy Akathisia Tremor Essential tremor Intention tremor Restless legs Stiff-person Dementia Alzheimer's Early-onset Primary progressive aphasia Frontotemporal dementia/Frontotemporal lobar degeneration Lewy body dementia Posterior cortical atrophy Creutzfeldt–Jakob disease Vascular dementia Mitochondrial disease Leigh syndrome Demyelinating Autoimmune Inflammatory Multiple sclerosis For more detailed coverage, see Template:Demyelinating diseases of CNS Episodic/ paroxysmal Seizures and epilepsy Focal Generalised Status epilepticus For more detailed coverage, see Template:Epilepsy Headache Migraine Cluster Tension For more detailed coverage, see Template:Headache Cerebrovascular TIA Stroke For more detailed coverage, see Template:Cerebrovascular diseases Other Sleep disorders For more detailed coverage, see Template:Sleep CSF Intracranial hypertension Hydrocephalus Normal pressure hydrocephalus Choroid plexus papilloma Idiopathic intracranial hypertension Cerebral edema Intracranial hypotension Other Brain herniation Reye syndrome Hepatic encephalopathy Toxic encephalopathy Hashimoto's encephalopathy Static encephalopathy Both/either Degenerative SA Friedreich's ataxia Ataxia–telangiectasia MND UMN only: Primary lateral sclerosis Pseudobulbar palsy Hereditary spastic paraplegia LMN only: Distal hereditary motor neuronopathies Spinal muscular atrophies SMA SMAX1 SMAX2 DSMA1 Congenital DSMA Spinal muscular atrophy with lower extremity predominance (SMALED) SMALED1 SMALED2A SMALED2B SMA-PCH SMA-PME Progressive muscular atrophy Progressive bulbar palsy Fazio–Londe Infantile progressive bulbar palsy both: Amyotrophic lateral sclerosis

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Adapted from the Wikipedia article [Synucleinopathy](https://en.wikipedia.org/wiki/Synucleinopathy) by Wikipedia contributors ([contributor history](https://en.wikipedia.org/wiki/Synucleinopathy?action=history)). Available under [Creative Commons Attribution-ShareAlike 4.0 International](https://creativecommons.org/licenses/by-sa/4.0/). Changes may have been made.